Background:The role of coronary microvascular disease and its impact on functional and energetic reserve in heart failure with preserved ejection fraction (HFpEF) remains unclear. We hypothesized that in response to submaximal pharmacologic stress (dobutamine), patients with HFpEF have impairment in left ventricular (LV) myocardial mechanical (external work [EW]), energetic (myocardial O₂ consumption [MVO₂]), and myocardial blood flow (MBF) reserve. We further assessed whether coupling of MBF to EW is impaired in HFpEF and associated with compensatory increases or pathological decreases in myocardial O₂ extraction. Lastly, we assessed whether coupling of MVO₂ to EW (mechanical efficiency) was impaired in HFpEF.Methods and Results:In prospectively enrolled patients with HFpEF (n=19) and age/sex-matched healthy controls (n=19), we performed ¹¹C-acetate positron emission tomography assessing MVO₂ and MBF at rest and during dobutamine infusion. EW was calculated as stroke volume (echo)×end-systolic pressure×heart rate. At rest, compared with controls, patients with HFpEF had higher LV EW, MVO₂, and MBF. With dobutamine, LV EW, MVO₂, and MBF increased in both HFpEF and controls; however, the magnitude of increases was significantly smaller in HFpEF. In both groups, MBF increased in relation to EW, but in HFpEF, the slope of the relationship was significantly smaller than in controls. Myocardial O₂ extraction was increased in HFpEF. Mechanical efficiency was similar in HFpEF and controls. In a post hoc analysis, HFpEF patients with LV hypertrophy (n=10) had significant reductions in LV mechanical efficiency relative to controls.Conclusions:In HFpEF during submaximal dobutamine stress, there is myocardial mechanical-, energetic- and flow-reserve dysfunction with impaired coupling of blood flow to demand and slight increases in myocardial O₂ extraction. These findings provide evidence that coronary microvascular dysfunction is present in HFpEF, limits O₂ supply relative to demand, and is associated with reserve dysfunction.

中文翻译：

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保留射血分数的心力衰竭心肌能量学。

背景：冠心病微血管疾病在保留射血分数（HFpEF）的心力衰竭中的作用及其对功能和能量储备的影响尚不清楚。我们假设响应最大药理压力（多巴酚丁胺），HFpEF患者的左心室（LV）心肌力学（外部工作[EW]），精力充沛（心肌O ₂消耗[MVO ₂ ]）和心肌血流受损（MBF）储备金。我们进一步评估了HFpEF中MBF与EW的结合是否受损，并与心肌O ₂提取的代偿性增加或病理性减少有关。最后，我们评估了MVO ₂是否偶联方法和结果：在前瞻性入选HFpEF（n = 19）和年龄/性别匹配的健康对照（n = 19）的患者中，我们进行了¹¹ C-乙酸正电子发射断层显像评估静息期间和多巴酚丁胺输注期间的MVO ₂和MBF。EW计算为中风量（回声）×收缩末压×心率。休息时，与对照组相比，HFpEF患者的LV EW，MVO ₂和MBF较高。使用多巴酚丁胺，LV EW，MVO ₂，而HFpEF和对照组的MBF均升高；但是，HFpEF的增加幅度明显较小。在两组中，MBF相对于EW均增加，但在HFpEF中，该关系的斜率显着小于对照组。HFpEF增加了心肌O _2的提取。HFpEF和对照组的机械效率相似。在事后分析中，HFpEF LV肥厚患者（n = 10）相对于对照组的LV机械效率明显降低。结论：在HFpEF中，多巴酚丁胺负荷低于最大时，存在心肌机械，能量和血流储备功能障碍，血流与需求的耦合受损，心肌O ₂轻微增加萃取。这些发现提供了证据，表明HFpEF中存在冠状动脉微血管功能障碍，相对于需求限制了O _2的供应，并与储备功能障碍有关。